Assessment of the cardiovascular system is one of the most complex and nuanced skills in the EMT’s repertoire, requiring a delicate blend of physical exam techniques, focused history questions and technologically derived data. A comprehensive assessment of the cardiovascular system is neither practical nor productive in the prehospital arena, but with an appropriate focused assessment, EMS providers can readily identify most cardiovascular emergencies. This article will focus on medical causes of cardiovascular instability.
A 64-year-old woman calls 9-1-1 complaining of food poisoning. EMTs find her sitting in a chair and retching into a wastebasket. She is pale and diaphoretic and appears acutely ill. She says she came home after dining out two hours ago and suddenly felt profoundly weak and nauseous. She denies chest pain or dyspnea, but reports a mild epigastric pain that she attributes to vomiting. She has non-insulin-dependent diabetes, hypertension and high cholesterol. She has no known drug allergies, and her only meds are lisinopril, Zocor and Actos.
Vital signs are:
- Heart rate 40, with irregular, palpable radial pulses
- Respirations 20 per minute, non-labored
- BP 108/56
- SpO2 98% on room air
- ECG rhythm sinus bradycardia, with occasional ventricular escape beats CBG 154 milligrams per deciliter
Having ruled out hypoglycemia, the medics suspect other possible causes of her symptoms, begin a focused assessment and obtain a 12-lead ECG.
Finding no immediate life threats, they move on to a history and physical examination, focusing on her chief complaint and associated signs and symptoms. The traditional format of OPQRST works well for assessment of cardiac problems:
Onset: What was the patient doing when the symptoms began? Symptoms occurring at rest indicate MI, while exertional symptoms point to angina; however, do not rule out MI based on the presence of exertional angina.
Provocation/Palliation: What makes the symptoms worse or better? Symptoms relieved by rest and nitroglycerin tend to indicate stable angina, while MI pain tends to persist despite these things. If dyspnea worsens when supine, a condition known as orthopnea, CHF may exist. If chest pain eases while leaning forward, this is a hallmark sign of pericarditis and can be confirmed by global ST-segment elevation on the 12-lead ECG.
Quality: Have the patient describe the symptoms in her own words. The pain of an MI is visceral pain that is often described as a vague heaviness, pressure or tightness. Somatic, musculoskeletal pain worsens with movement and can often be reproduced by palpation. Pleuritic pain often worsens with coughing or deep inspiration, is an example of parietal pain that occurs in the body cavity linings richly innervated with sensory fibers, and is usually described as “sharp” or “stabbing” and defined in one part of the body.
The presence of pleuritic pain does not rule out MI. As many as 15% of MI patients, particularly women, present with pleuritic chest pain.
Radiation: Visceral organs share sensory nerve roots, so ischemic chest pain may radiate to other areas of the body, particularly the left arm, shoulders, jaw and neck. Since the inferior wall of the left ventricle shares sensory innervations with the diaphragm, patients experiencing inferior wall MI often present with epigastric pain, indigestion or, in rare instances, hiccups.
Severity: Ask the patient to rate the pain on a 1–10 scale. Pain measurement is purely subjective but provides a baseline for measuring the effectiveness of nitroglycerin or morphine.
Time: Ask the patient when symptoms began. MI patients commonly deny the possibility of a heart attack and delay seeking help.
Diagnosing Cardiac Pain
Now, what clues might lead us to suspect that her chief complaint is due to a cardiac problem?
The answer lies in two words: anginal equivalents. Up to 30% of myocardial infarction patients suffer no chest pain during the event. While the “silent MI” is a truly rare phenomenon and may indeed not even exist, patients who suffer no chest pain during MI almost always experience one or more of a constellation of easily identifiable symptoms: sudden onset of dyspnea, profound weakness or dizziness, or nausea and vomiting. These symptoms are known as anginal equivalents.
Patients suffering these atypical signs are more likely to be elderly, female or diabetic, but anginal equivalents occur across the demographic spectrum. When assessing a patient with known risk factors for cardiovascular disease, consider MI until proved otherwise.
The 12-lead ECG reveals 3mm ST-segment elevation in leads II, III and AVF. Focused examination reveals clear lung sounds, absence of pedal edema or clubbing, and mild jugular venous distension that seems to worsen upon inspiration. When she stands up to get on the stretcher, she passes out.
The EKG findings indicate an inferior wall MI. Blood flow to the inferior wall of the left ventricle is supplied by the right coronary artery, the proximal branches of which also supply the right ventricle. If the occlusion is high in the RCA, blood flow to the right ventricle is compromised as well. Patients with right ventricular infarction are extremely susceptible to changes in preload, and relatively small doses of vasodilators like nitroglycerin may induce profound hypotension and further compromise coronary blood flow.
The patient’s orthostatic syncope is a clue that she is preload-dependent, as is the presence of JVD with clear lung fields, a finding known as Kussmaul’s sign. Normally, we would expect to find evidence of pulmonary edema in the presence of JVD, and venous distension usually decreases with inspiration. However, in patients with Kussmaul’s sign, a stiff, non-compliant right ventricle—in this case from infarction—impairs right ventricular filling, and JVD often increases with inspiration instead of decreasing.
Suspecting a right ventricular infarction, the medics obtain a second 12-lead ECG, this time with the V3 and V4 leads placed in mirror image on the right side of the chest. The two leads, known as V3R and V4R, also show 2mm ST-segment elevation, confirming the presence of a right ventricular infarction. They initiate immediate transport to the chest pain center, call a STEMI alert to activate the cath lab team, administer 324 mg aspirin and establish IV access. They withhold nitroglycerin until the IV is started so they can bolus the patient if her blood pressure drops.
ST-elevation myocardial infarction, or STEMI, occurs when an occlusion of coronary arteries, most commonly by a clot formed over a ruptured atherosclerotic plaque, deprives a portion of the myocardium of oxygenated blood. The process begins with tissue becoming ischemic, then injured and finally infarcted. Ischemia and injury are reversible processes, while infarcted tissue is unsalvageable.
Since ischemic or injured tissue tends to remain partially polarized or depolarized, we can recognize those processes in the ST-segments and T-waves of a 12-lead ECG. Ischemic tissue tends to manifest itself as T-wave inversion or ST-segment depression in the leads viewing the affected myocardium. This unstable angina, or non-ST-elevation MI (NSTEMI), along with STEMI and acute pulmonary edema, make up the acute coronary syndromes.
NSTEMI and unstable angina are indistinguishable clinically; all should be transported to an accredited chest pain center if one is available. Automatic cath lab activation, however, is usually limited to those patients suffering from STEMI. Twelve-lead ECGs are not infallible and may fail to recognize a significant number of STEMI patients. Since the traditional 12-lead ECG only views the left ventricle, medics may also obtain a 15- or 18-lead ECG to identify posterior wall MI or, in this case, right-sided chest leads to rule out RVI.
Dysrhythmias are a frequent complication of cardiac events. Generally speaking, these abnormal rhythms are only treated in the prehospital arena if they herald impending cardiovascular collapse, or if they induce hemodynamic instability.
Bradycardia in the MI patient, particularly resulting from high-degree AV blocks, may indicate significant damage to the cardiac conduction system. In our patient who exhibits an intact conduction system with sinus bradycardia, however, the slow heart rate may be due to a cardioprotective reflex known as the Bezold-Jarisch reflex. Bradycardia in MI patients should not be treated unless it results in hemodynamic instability.
Congestive heart failure can be chronic or can occur acutely from MI. If acute, classic signs of CHF such as ascites and pedal edema may not be present. Jugular venous distension is often noted, accompanied by pulmonary edema, and an S3 heart sound may be heard.
Normal heart sounds (S1 and S2) are produced by closing of the atrioventricular and semilunar valves, respectively. In the CHF patient, a third heart sound (S3) may be heard by auscultating with the bell side of the stethoscope over the fifth intercostal space at the left sternal border. The S3 sound occurs during diastole, and is heard after S1 and S2. The auditory pattern, different from the normal “lub dub” S1-S2 pattern, is often described as Kentucky (KEN-TUH-kee), with emphasis on the first two syllables because the S3 sound is lower in pitch than S1 or S2.
Assessing the patient with cardiac complaints can be challenging. EMTs should obtain a thorough, complaint-focused history and physical exam, augmented by technological assessment like a 12-, 15- or 18-lead ECG. Even in the presence of a non-diagnostic or normal ECG, the patient’s presenting chief complaint, history and exam findings may yield valuable clues to his or her condition. Patients with acute coronary syndromes should be identified early and transported to an accredited chest pain center or ED with a 24-hour cardiac cath lab. Diagnosis of these syndromes is not made solely from lab tests or ECG criteria; the entire clinical picture is important.
Steven “Kelly” Grayson, NREMT-P, CCEMT-P, is a critical care paramedic for Acadian Ambulance in Louisiana. He has spent the past 14 years as a field paramedic, critical care transport paramedic, field supervisor and educator. He is the author of the book En Route: A Paramedic’s Stories of Life, Death, and Everything In Between, and the popular blog A Day in the Life of An Ambulance Driver.
William E. (Gene) Gandy, JD, LP, has been a paramedic and EMS educator for over 30 years. He has implemented a two-year associate’s degree paramedic program for a community college, served as both a volunteer and paid paramedic, and practiced in both rural and urban settings. He lives in Tucson, AZ.